Thromboxane A.sub.2 (TxA.sub.2) is a potent, unstable biosynthetic product of arachidonic acid. It is a very potent platelet aggregating, vasoconstricting and bronchoconstricting agent. Inasmuch as these properties could be harmful to an organism, compounds which could inhibit thromboxane synthetase and thereby inhibit formation of thromboxane A.sub.2 could be of importance. Thus, for example, imidazole has been shown to be a specific inhibitor of thromboxane synthetase. Nijkamp et al., "Diversion of Prostaglandin Endoperoxide Metabolism by Selective Inhibition of Thromboxane A.sub.2 Biosynthesis in Lung, Spleen or Platelets", Europ, J. Pharmacol., 44:179-186, (1977); Moncada et al, "Imidazole: A Selective Inhibitor of Thromboxane Synthetase" (1977) Prostaglandins 13, 611-618 and Tai et al. "On the Inhibitory Potency of Imidazole and its Derivatives on Thromboxane Synthetase", Biochem. and Biophys. Res. Commun. 80:236-242 (1978) disclose that 2-, 4- and 6-substituted imidazoles are inactive while 1-substituted imidazoles wherein the substituent is alkyl, benzyl and 2-isopropylphenyl are inhibitors of thromboxane synthetase formation.
Yoshimoto et al, "Selective Inhibition of Prostaglandin Endoperoxide Thromboxane Isomerase by 1-Carboxyalkylimidazoles", (1978), Prostaglandins, 16, 529-540 disclose that 1-carboxyalkylimidazoles and 1-alkylimidazoles are inhibitors of the conversion of prostaglandin H.sub.2 to thromboxane B.sub.2.
Selective inhibitors of thromboxane synthetase have potential in the prevention of myocardial ischemia, angina pectoris, myocardial infarction, stroke and transient ischemic attacks, diabetes, intravascular inflammation, asthma, anaphylactic shock, atheroschlerosis, endotoxin shock, certain viral conditions, and systemic and pulmonary hypertension.